The most frequent alteration in the prostate oncogenome is loss of chromosome (chr) 8p21 that has been associated with loss of NKX3.1 homeobox gene.

Huh? What?

The statement above is the first sentence in the abstract of a new paper by Bucay et al. in the journal Cell Death and Differentiation. However, …

What this paper is really about is whether a particular subtype of micro-ribonucleic acid known as miR-3622a does or doesn’t have a truly crucial role in the epithelial-to-mesenchymal transition (EMT) of prostate cancer cells that allows those prostate cancer cells to metastasize at all … and whether we could actually stop that EMT from occurring.

This paper illustrates just how difficult it is to know what to report about to patients about the future of treatment of prostate cancer.

Normally, we don’t worry too much about data from this type of “early science”. We simply wait to see whether ideas like this come to fruition (which can take years). But this paper might, in fact, be very important indeed to the future of the treatment of prostate cancer. The authors are correct when they state that their latest data continue to support “a novel, paradigm shifting hypothesis” about how prostate cancer progresses over time.

However, there is a huge spectrum of “ifs” and “maybes” that will need to all be negotiated before we will be able to know (a) whether their hypothesis is correct and (b) whether we can actually take advantage of this hypothesis to actually shut down the EMT pathway that allows prostate cancer to metastasize.

First, we will need to know just how accurately the expression and down-regulation of the expression of miR-3622a is correlated with tumor progression and patient survival in real, high-risk prostate cancer patients with early stage disease. If we know that, then it may be possible to use the degree of regulation of miR-3622a as a test for risk for metastatic prostate cancer.

Second, we will need to know if there are ways to stop the down-regulation of the expression of miR-3622a (so that this biochemical continues to be expressed at normal levels) and whether stopping such down-regulation really does stop — or at least significantly delay — the onset of EMT and thus the initiation of prostate cancer metastasis.

Third, if we can indeed find a way to stop the down-regulation of miR-3622a, and if we can find a way to make that methodology easily available to patients (though some sort of drug), we would then have to be able to prove that such a treatment was both effective and safe for the patients (and thus be able to get the treatment approved by the U.S. Food & Drug Administration and other regulatory authorities around the world).

None of those three steps along the medical-scientific “translational pathway” will be easy. But the idea is enticing. Otherwise your sitemaster would never have written this commentary!

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